Numerous mouse genes involved in virus-induced neoplastic disease have been identified in genetic studies. These genes include endogenous retroviral sequences as well as mouse cellular genes which facilitate or inhibit virus replication. We used the human gene for the gibbon ape leukemia virus (GALV) receptor to identify homologous sequences in the mouse, and we also identified multiple copies of GALV-related sequences in the mouse genome suggesting that this gene may have functioned as a receptor in the evolution of Mus. Our genetic mapping of this sequence also suggested possible identity with Rec-2, the Chr 2 encoded receptor for a wild mouse retrovirus. In other experiments we characterized three common viral integration regions associated with tumor induction, demonstrating that one represents a novel gene, and one represents a site previously shown to be rearranged following integration by a different virus and resulting in a different disease type. We also demonstrated that the Fv-2 resistance locus does not encode the erythropoietin receptor, but identified a genomic sequence which maps at or near this resistance gene. Finally, we have used site specific mutagenesis to alter the site in the p30 gag region of the AKV MuLV which is thought to interact with the gene product of the Fv-1 resistance gene.